Benefits in Acute Heart Failure - Essay Example

Module Why Have So Many Randomized Controlled Trails Failed To Show Benefits in Acute Heart Failure? Number Submission Date Table of Contents Abstract 3 Introduction 4 Definition 4 Etiology 4 Epidemiology 5 Treatment 6 Review on failure in acute heart failure random trials 6 References 14 Abstract Heart failure (HF) is an increasing global problem: more than twenty million individuals around the globe are affected, and over seven million people in the Western countries (35, 39, and 40). The occurrence of HF rests on an exponential outline which rises with progression in age (35). The prevalence of heart failure in persons over sixty-five years is six to ten percent. The relative incidence of heart failure is lower in women than in men, but women patients make up to around fifty percent of the incidences of heart failure owing to their prolonged life expectancy (35, 13). Heart failure treatments have recently risen with the increase of heart failure incidences. The Journal of Cardiac Failure (35) estimates that heart failure treatment represents about 2to 3% of the whole treatment expenditures. Hospitalizations and emergency treatments take the larger share of these costs (35, 27, 21, and 13). Over thirty million people are diagnosed with heart failure as a secondary diagnosis (35, 11, 14, and 26). Heart failure is the most incriminated cause of hospitalization of patients aged sixty five years and above (26, 35). The occurrence of heart failure illnesses in the western nations has tripled over the past three decades as a consequence of a large aging society. Hospital admissions with acute decompensated heart failure or ADHF predict readmissions and post-discharge mortalities (up to 40%) in persons with chronic heart failure (27, 36). Readmissions are related to the large aging population, better survival after myocardial infarction, and extended survival of heart failure victims through modern device and medical therapies (35). Nevertheless, the current therapies are not fully promising. Various medical treatments have lead to poor health, hospital readmissions, other post-treatment complications, and even death (20, 28). The rate failure of these types of treatments is very high due to various underlying reasons (38). Introduction Definition Gheorghiade (2) defines heart failure as a medical disorder exemplified by systemic perfusion insufficient to attain the body’s metabolic requirements due to weakened cardiac pump function. It manifests itself in two different ways, diastolic or systolic heart failure involving weakened cardiac relaxation and irregular ventricular filling; and diminished cardiac contractility respectively (8). Etiology Left ventricular (LV) systolic malfunction is the most incriminated cause of heart failure constituting about sixty percent of the cases (6). Most patients end up with this complication due to pre-established coronary artery disease, with cases of myocardial infarction or persistently under -perfused viable myocardium. Both complications are common in most of the patients (9). LV dysfunction may also be caused by other conditions including hypertensive heart disease, valvular heart disease, congenital heart disease, idiopathic dilated cardiomyopathy, and toxin-generated cardiomyopathies such as alcohol and doxorubicin (2, 3, 7). LV systolic dysfunction causes the right ventricular systolic failure (8). Pulmonary hypertension, right ventricular dysfunction, arrhythmogenic right ventricular enlargement, and persistent severe tricuspid back flow are other possible causes (1). Other minor causes include arteriovenous fistulae, Paget’s disease, severe chronic anemia, pregnancy and thyrotoxicosis resulting to high-output failure with a consequent the dysfunction. Diastolic LV failure or impaired relaxation is linked to ischemic heart disease or persistent hypertension (8). Minor causes include infiltrative, restrictive, and hypertrophic cardiomyopathies. Inadequate filling is caused by pericardial constriction and cardiac tamponade. Epidemiology Heart failure is a more common illness in the older population than in younger counterparts (6). Many people survive acute myocardial infarction through reperfusion therapy, but they are at high risk of heart attack due to residual LV systolic dysfunction (9, 5, 1). Approximately 2% of England’s population is affected by heart failure (35). About one million of patients who are admitted in hospitals suffer from heart failure. About one and half million patients have been diagnosed with the complication as a secondary diagnosis (4). Hypertension, diabetes mellitus, cardiotoxin users, obese, family line of cardiomyopathy, and coronary artery diseases are risk factors for the development of heart failure. Pathophysiology LV systolic dysfunction is characterized by a series of physiological processes (41). Neurohormonal pathways are stimulated to amplify circulating blood volume (3). The sympathetic nervous system amplifies heart rate and contraction, initiate arterial-vasoconstriction in nonessential vessel beds and initiates discharge of renin from the kidney juxtaglomerular apparatus (6, 7). Unluckily, catecholamines exacerbate ischemia, increase arrhythmias, promote cardiac remodeling and intoxicate heart muscle cells. Activation of renin-angiotensin system by the increased sympathetic stimulation and reduced renal perfusion causes further arterial-vasoconstriction, water and sodium retention, and secretion of aldosterone (9, 11, 14). Elevated aldosterone levels results into further water and sodium retention, endothelial dysfunction and myocardial fibrosis (19). The hypothalamus releases vasopressin through stimulation by baroreceptor and osmotic stimulus with a resultant reabsorption of water by the renal collecting tube. These are beneficial compensatory neurohormonal pathways but later turn lethal. Modern methods of treatment of cardiac failure rely on these pathways (36, 7). In response to myocardial stretching, the myocytes release natriuretic peptides (18-22, 28, 10). These cause beneficial cardiac changes such as facilitation of water and sodium excretion, systemic and pulmonary vasodilation, and inhibition of other neurohormones (19). Treatment A number of drugs have been in use to abate symptoms and extend survival of heart failure patients (17-23, 29, 32). These drugs are utilized in the remedy of specific symptoms and work in different mechanisms based on their mode of action and predilection site (27, 6). Medications in use include beta blockers e.g. carvedilol and Bisoprolol, diuretics e.g. butamedine and furosemide, ACE inhibitors e.g. quinapril and Fosinopril (17-32). Angiotensin II receptor blockers (ARB) e.g. candesartan and valsartan, aldosterone antagonists e.g. spironolactone and eplerenone, hydralazine-isosorbide nitrate combination and digoxin e.g. Lanoxin (17-32, 12, 3).These drugs have shown differences in success, in different patients. Patient tolerance to these medications is also diverse among the population of patients (10, 28, 31). Patients have succumbed to the illness even with persistent treatments with these drugs. The level of hospital readmission is considerably high, even up to forty percent with some drugs (15, 26, 30). This has prompted the necessity to research and quantify the ability of various drugs to treat acute heart failure (19, 15). Review on failure in acute heart failure random trials The Acute Decompensated Heart Failure National Registry (ADHERE) database contained 147,362 records by December 2004 (21, 22). Seventy eight percent had cases of acute decompensated cardiac failure. Of these, thirty-three percent had procedure data and aeration was used in 6.5%. In ventilated patients 72.4% received noninvasive ventilation or NIV and 27.6 received endotracheal intubation or ETI without NIV. In the NIV group, 95.9% were managed exclusively by NIV (NIV success), and 4.1% failed NIV and hence were treated with ETI (NIV failure) (21, 22). Higher values of atrial fibrillation, heart failure and COPD were registered in the NIV success cohort in comparison to the ETI cohort (p< 0.05 for all). The higher number in the ETI success had liver failure there were no variations in the past medical history in comparison to the study ETI group (21). The hemodynamics data demonstrated that NIV failures looked like ETI cohort more than NIV victory (2). Only oxygen saturation (SaO2) varied in the NI failure and ETI, with the lowest extent (84%) in the NIV failure group and highest (90%) in NIV success group. Levels of volume overload were diverse in the NIV success and ETI No differences were recorded in chest x-ray congestion rales, though edema and rales were higher frequent, and dyspnoea at relaxation less frequent in the NIV success cohort. NIV failures had a lower level of abnormal troponin concentration than the ETI cohort (7% versus 13%) The most extrapolative parameters for death, creatinine, systolic blood pressure, and blood urea nitrogen or BUN were parallel among all cohorts (2, 20, 21). Intravenous medications administered during hospitalization recorded less difference in NIV failure and ETI beyond that of NIV success and ETI failure (22). To facilitate respiration in patients with failing airways, NIV cohort received equal amounts of ionotropes but a higher rate of vasodilators than their counterparts in the ETI group (32). ETI patients were administered with more vasoactives except for nesiritide (2). Urgency of treatment is very essential in dyspnea and it is of importance noting existence of negligible differences in time to vasoactives within the ventilation cohorts (21). Nevertheless, NIV failures and success established intravenous diuretics at a faster rate than the ETI cohort (18 minutes versus 36 minutes respectively) NIV failures had less dialysis, CPR, and defibrillation than ETI. The observation was consistent with decreasing disease severity, important in NIV success and no ventilation cohorts against ETI (21, 17). Gheorghidae’s et al (21) study is an assessment of an enormous retrospective data collection and cannot establish trigger and effect. It is imperative to identify that doctors employ a medley bias while preferring immediate ETI or NIV for ADHF (33).The little number of NIV malfunction (less than 5%) is constant with an elevated degree of precision in choosing the appropriate patient. It is inevitable to notice that an important number of patients are in need of immediate ETI, and we are not able to point out on the outcomes (26, 20). We should also observe that a considerable number of patients needed immediate ETI (28%), hence we should not comment on the importance of NIV in this group. Furthermore, though it seems that ETI patients had a larger severity of disease, as witnessed by the augmented risk of unpleasant outcomes, we cannot establish if the assortment of patients for instant ETI was correct or appropriate (20, 2). Some who obtained instant ETI might have been effectively managed with NIV. However, with the proposition that the test of NIV never considerably increase the risk in ADHF, a potential analysis to find out if NIV develops out-comes can be practically performed (33). Instead, our results could be prejudiced by the effect of reduced severity of sickness in the NIV success group, where doctors used NIV in individuals who did not need it (20, 32). This is not backed by the population, the initial presentation, or persistent treatment data. While there were important variations in the medical account, four of the five limits were essentially bad in the NIV success group, as compared to ETI (18, 31). In another study testing findings related to acute mortality, an original BUN >43mg/dL, systolic blood pressure < 115mmHg, or creatinine above 2.7mg/dL was the most significant predictor of death. Gheorghidea (21) reported no difference in the NIV success and the ETI cohorts. Lastly, when troponin rise has been noted to be more rampant in NIV and the period of treatment was uneven because of biased judgment by the physician (33). The timing of definite start of NIV and ETI was not set and was at the judgment of the treatment expert. The phenomenon makes timing a constraint (38). Furthermore, patients involved in this study resided in different localities, in the holding hospital facility and not restricted in the emergency department or observation unit (30). Procedures were performed in the experiment department and there are no recorded details on precise timing or duration (33, 2). Based on this information there is a possibility of failure to arise in any tests or treatment that were done in the manner. No stage can be easily rectified to yield desirable results since the whole process is marred with ill practices involving overlooking or ignorance of important factors such as recording start times and durations (22, 30, 33, 40). Huiskes and Dracup (26) indicate that lack of intensive patient education and follow-up programs which use home care services affected the improvement of discharged patients. The follow up is meant to assist the patient work positively on their therapy and evaluate the progress. Assessments allow for necessary rectifications thereby saving the patient looming risks of deteriorating health. Aronson (36) potentiates this concept blaming the lack of moral support from the physician kills the slightest hope of recovery. Parore (40) says that lack of following up leads to bad practices. Patients with little or no follow-up may sometimes skip or fail to take their medicines, take less or higher doses than prescribed and may even completely cease taking the medications (10-18, 26, 28). Lack of contacts both with the patients and physician as indicated by Gheorghiade (20) has been seen to affect the effectiveness of treatment of acute heart failure. Contacts including telephone or personal visits are essential in assessing the progress of the effectiveness of treatment in acute heart failure patients. Some patients are located in unreachable areas with difficulty of contacts. A twenty four-hour telephone service should be provided to allow patients to convey any message of their progress to their physicians (26, 27). Other patients in remote areas cannot easily access health facilities for periodic checkups to quantify the effect of the drug in use and the progression health. Others cannot economically afford the required medications and other accessories such as special foods (33, 35). Nicol et al (30) relates failure of action of the acute heart failure trials from lack of adherence to the prescribed regulations. Some patients such as those who take alcohol are not keen enough or through their addiction succumb to taking alcohol that should be kept off since it is one of the cardiotoxins. Werns (32) says that the healing effects are counteracted by the new injury imposed by the intake of the toxins and the Journal of Cardiac Failure (35, 33) emphasizes that the illness may even be exacerbated due to the hostile interaction of the drug and the toxin. Moser’s (15) work was limited by several factors. First, the plan was multidisciplinary not designed to assess the comparative roles of its different components (9). Secondly, physicians attending to the patients in the nonintervention cohort received specialist recommendations at the moment that the patients had already been discharged from hospital and discovered that their patients were in randomized trials evaluating acute heart failure treatment (10, 12, 16). This assessment was not to the true common care cohort thus increasing the chances that these factors could have influenced the rate of event in the nonintervention section (14, 18, 20). Gheorghiade (20, 21) says that the third factor could be that some of the secondary results were taken in an unblinded way by the patients’ attendant. According to Howlett (25), not all tools that were used to measure medications and dietary observance were validated. This raises the chances of biases in the unblinded resultant end points. Gheorghiade et al (21) and Givert (23) gave a fourth reason that the results might not be applicable to all of the assessed patients, because the study purposely targets patients considered to be at an elevated risk of readmission. Aoyama (17) concludes with the proposition that not all patients with acute heart failure are in need of such an intervention. It is difficult to determine which patient cohorts benefited from participation, according to the data collected. Summers et al (31) warn that many commercial acute heart failure management do not engage cardiologists or professional nurses in their undertakings but base their conduit on telephone management alone. From the data provided, it is vague to determine whether telephone management on its own yields any benefits (33). Colquhoun and Ferreira (37) point out that an effective study would require that those analyzing the results should determine the patient cohorts that benefit most in such an intervention. In the Journal of Cardiac Failure (35) and the European Journal of Heart Failure Supplements (30) the authors agree that deciding the prognosis of heart failure is complex. Huiskes and Dracup (26) bring forth that diverse etiologies, frequent co-morbidities, age, and differences in individual sequence and effects e.g. sudden against progressive heart failure death should be considered. According to Kuhl (28) and Kramer (39), the impact on recovery of particular treatments is usually hard to predict. The differences on a larger extent represent specialist compromise opinion without documentation (33, 30). Adherence to treatment (12, 19, 22) show difference with the degree achievements. Adherence is directly proportional to the success of prognosis (29, 31, 32). Good adherence decreases morbidity and mortality consequently improving well-being (20). Literature on adherence to treatment reveals that around 40-60% of patients suffering from acute heart failure do not stick to their recommended non-pharmacologic and pharmacologic treatment (26, 33, 36 39). This is related to patient’s lack of understanding, failure to recall or the patients’ leniency. Craig and Stitzel (38) indicate that a poor relationship between physicians and patients plus lack of sufficient social backing affects the adherence. Georghiade (20) recommends that kinfolks should be involved in the treatment care and education programs. (10- 16) potentiate the proposition indicating the necessity of providing patients with adequate knowledge on their illness and treatment. Patients with no knowledge of treatment effects, side effects plus guidelines on how to take or titrate the medication. Colquhoun and Ferreira (37) show that training patients possessing cognitive problems would be difficult and might yield limited results. Failure is also related to the patients’ high expectations that effects will be immediate and enormous (38, 30, 21). Such unrealistic expectations should be removed through proper training and guidance. According to Howlett (25), most patients do not expect the side effects of medications. These may end up despairing and abandon treatment. Lewis (29) suggests that failure of the physicians to guide their patients on what to expect has adversely affected success and prognosis in acute cardiac failure in most patients (28, 30, 33). In their work, Huiskes and Dracup (26) blame the lack of healthcare providers to develop interventions that would improve adherence to treatments. Conclusion Heart failure is an alarming disease for which extensive research has been undertaken. With the current rate of morbidity at a high rate, both in new and existing cases, and high post-treatment mortality rate, more should be done to provide new remedies or improve the performance of existing ones (2, 41). As learnt, extensive studies should be probed into to elucidate all underlying causes of the disease, its reoccurrence, and relationship with other systems and illnesses (41). With the high rate of mortality the disease should be extensively be conducted to preempt the looming risks of infections or sudden deaths. References 1. Connor, C. 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